Controlled Mechanical Ventilation in Critically Ill Patients and the Potential Role of Venous Bagging in Acute Kidney Injury.

A very low incidence of acute kidney injury (AKI) has been observed in COVID-19 patients purposefully treated with early pressure support ventilation (PSV) compared to those receiving mainly controlled ventilation. The prevention of subdiaphragmatic venous congestion through limited fluid intake and the lowering of intrathoracic pressure is a possible and attractive explanation for this observed phenomenon. Both venous congestion, or "venous bagging", and a positive fluid balance correlate with the occurrence of AKI. The impact of PSV on venous return, in addition to the effects of limiting intravenous fluids, may, at least in part, explain this even more clearly when there is no primary kidney disease or the presence of nephrotoxins. Optimizing the patient-ventilator interaction in PSV is challenging, in part because of the need for the ongoing titration of sedatives and opioids. The known benefits include improved ventilation/perfusion matching and reduced ventilator time. Furthermore, conservative fluid management positively influences cognitive and psychiatric morbidities in ICU patients and survivors. Here, it is hypothesized that cranial lymphatic congestion in relation to a more positive intrathoracic pressure, i.e., in patients predominantly treated with controlled mechanical ventilation (CMV), is a contributing risk factor for ICU delirium. No studies have addressed the question of how PSV can limit AKI, nor are there studies providing high-level evidence relating controlled mechanical ventilation to AKI. For this perspective article, we discuss studies in the literature demonstrating the effects of venous congestion leading to AKI. We aim to shed light on early PSV as a preventive measure, especially for the development of AKI and ICU delirium and emphasize the need for further research in this domain.

Mean systemic filling pressure and venous return to assess the effects of passive leg raising and volume expansion in acute circulatory failure patients: a posthoc analysis of a multi-centre prospective study.

BACKGROUND: The main aim of the study was to investigate the behaviours of the mean systemic filling pressure (Pmsf), calculated by the mathematical method, and its derived variables of venous return after volume expansion (VE) and passive leg raising (PLR), with analysis according to fluid and PLR responsiveness. METHODS: This was a post-hoc analysis of a multicentre prospective study. We included 202 mechanically ventilated patients with acute circulatory failure. Pmsf, dVR (difference between Pmsf and central venous pressure [CVP]), and resistance to venous return (RVR) were calculated before/after PLR and before/after VE. Fluid- and PLR-responsiveness were defined according to the increase in cardiac index (CI) >15% after VE and >10% after PLR, respectively. RESULTS: Pmsf increased significantly after VE and PLR in both fluid and PLR-responder and non-responder groups. In fluid-responder patients, the increase in dVR was significantly higher than in non-responder group (1.5 [IQR:1.0-2.0] vs. 0.3 [IQR:-0.1-0.6] mmHg, p < 0.001) because of the larger increase in CVP relative to Pmsf in the non-responder group. The same findings were observed after PLR. RVR significantly decreased only in the fluid-responder and PLR-responder groups after VE and PLR. CONCLUSIONS: Venous return, derived from the mathematical model, increased in preload-dependent patients after VE and PLR because of the larger increases in Pmsf relative to CVP and the decreases in RVR. In preload-independent patients, VR did not change because of the larger rise in CVP compared to Pmsf after VE and PLR. These findings agree with the physiological model of circulation described by Guyton.

Volume responsiveness revisited: an observational multicenter study of continuous versus binary outcomes combining echocardiography and venous return physiology.

Echocardiography can assess cardiac preload when fluid administration is used to treat acute circulatory failure. Changes in stroke volume (SV) are inherently a continuous phenomenon relating to the pressure gradient for venous return (VRdP). However, most clinical studies have applied a binary definition based on a fractional change in SV. This study tested the hypothesis that calculating the analog mean systemic filling pressure (Pmsa) and VRdP would enhance echocardiography to describe SV responses to a preload challenge. We investigated 540 (379 males) patients during a standardized passive leg raising (PLR) maneuver. Patients were further categorized by the presence of impaired right ventricular function (impRV) or increased intra-abdominal hypertension (IAH). Multivariable linear regression identified VRdP (partial r = -0.26, P < 0.001), ventilatory-induced variations in superior vena cava diameter (partial r = 0.43, P < 0.001), and left ventricular outflow tract maximum-Doppler velocity (partial r = 0.13, P < 0.001) as independent variables associated with SV changes. The model explained 38% (P < 0.001) of the SV change in the whole cohort and 64% (P < 0.001) when excluding patients with impRV or IAH. The correlation between Pmsa or VRdP and SV changes lost statistical significance with increasing impRV or IAH. A binary definition of volume responsiveness (>10% increase in SV) generated an area under the curve of 0.79 (P < 0.001) in logistic regression but failed to identify Pmsa or VRdP as independent variables and overlooked the confounding influence of impRV and IAH. In conclusion, venous return physiology may enhance echocardiographic assessments of volume responsiveness, which should be based on continuous changes in stroke volume.NEW & NOTEWORTHY The analog mean systemic filling pressure and the pressure gradient for venous return combined with echocardiography predict continuous changes in stroke volume following a passive leg raising maneuver. The confounding effects of impaired right ventricular function and increased intra-abdominal pressure can be identified. Using a binary cutoff for the fractional change in stroke volume, common in previous clinical research, fails to identify the importance of variables relevant to venous return physiology and confounding conditions.

Assessing the venous system: Correlation of mean systemic filling pressure with the venous excess ultrasound grading system in cardiac surgery.

BACKGROUND: Evaluation of the venous system has long been underestimated as an important component of the circulatory system. As systemic venous pressure increases, the perfusion pressure to the tissues is compromised. During initial resuscitation in cardiac surgery, excessive fluid administration is associated with increased morbidity and mortality. METHODS: We conducted a cross-sectional study of 60 consecutive adult patients who underwent cardiac surgery and in whom it was possible to obtain the venous excess ultrasound (VExUS) grading system and mean systemic filling pressure (Pmsf) in the postoperative period upon admission, at 24 and 48 h. We then determined the correlation between VExUS grading and Pmsf. RESULTS: On admission, patients with VExUS grading 0 predominated, with a progressive increase in venous congestion and an increase in Pmsf over the course of the first 48 h. There was a strong positive correlation between VExUS grading and the invasive measurement of Pmsf at 24 and 48 h after arrival. The presence of grade 2 or grade 3 venous congestion in the postoperative period poses an increased risk of developing acute kidney injury. CONCLUSION: The VExUS grading system indicates a high degree of systemic venous congestion in the first 48 h of the postoperative period after cardiac surgery and correlates with the Pmsf, which is the best surrogate of stressed circulatory volume.

Changes in mean systemic filling pressure as an estimate of hemodynamic response to anesthesia induction using propofol.

BACKGROUND: Even a small change in the pressure gradient between the venous system and the right atrium can have significant hemodynamic effects. Mean systemic filling pressure (MSFP) is the driving force of the venous system. As a result, MSFP has a significant effect on cardiac output. We aimed to test the hypothesis that the hemodynamic instability during induction of general anesthesia by intravenous propofol administration is caused by changes in MSFP. METHODS: We prospectively collected data from 15 patients undergoing major surgery requiring invasive hemodynamic monitoring. Hemodynamic parameters, including MSFP, were measured before and after propofol administration and following intubation, using venous return curves at a no-flow state induced by a pneumatic tourniquet. RESULTS: A significant decrease in MSFP was observed in all study patients after propofol administration (median (IQR) pressure 17 (9) mmHg compared with 25 (7) before propofol administration, p = 0.001). The pressure gradient for venous return (MSFP - central venous pressure; CVP) also decreased following propofol administration from 19 (8) to 12 (6) mmHg, p = 0.001. Central venous pressure did not change. CONCLUSIONS: These results support the hypothesis that induction of anesthesia with propofol causes a marked reduction in MSFP. A possible mechanism of propofol-induced hypotension is reduction in preload due to a decrease in the venous vasomotor tone.

Venous return and mean systemic filling pressure: physiology and clinical applications.

Venous return is the flow of blood from the systemic venous network towards the right heart. At steady state, venous return equals cardiac output, as the venous and arterial systems operate in series. However, unlike the arterial one, the venous network is a capacitive system with a high compliance. It includes a part of unstressed blood, which is a reservoir that can be recruited via sympathetic endogenous or exogenous stimulation. Guyton's model describes the three determinants of venous return: the mean systemic filling pressure, the right atrial pressure and the resistance to venous return. Recently, new methods have been developed to explore such determinants at the bedside. In this narrative review, after a reminder about Guyton's model and current methods used to investigate it, we emphasize how Guyton's physiology helps understand the effects on cardiac output of common treatments used in critically ill patients.

Analogue Mean Systemic Filling Pressure: a New Volume Management Approach During Percutaneous Left Ventricular Assist Device Therapy.

The absence of an accepted gold standard to estimate volume status is an obstacle for optimal management of left ventricular assist devices (LVADs). The applicability of the analogue mean systemic filling pressure (Pmsa) as a surrogate of the mean circulatory pressure to estimate volume status for patients with LVADs has not been investigated. Variability of flows generated by the Impella CP, a temporary LVAD, should have no physiological impact on fluid status. This translational interventional ovine study demonstrated that Pmsa did not change with variable circulatory flows induced by a continuous flow LVAD (the average dynamic increase in Pmsa of 0.20 ± 0.95 mmHg from zero to maximal Impella flow was not significant (p = 0.68)), confirming applicability of the human Pmsa equation for an ovine LVAD model. The study opens new directions for future translational and human investigations of fluid management using Pmsa for patients with temporary LVADs.

Experimental validation of a mean systemic pressure analog against zero-flow measurements in porcine VA-ECMO.

The mean systemic pressure analog (Pmsa), calculated from running hemodynamic data, estimates mean systemic filling pressure (MSFP). This post hoc study used data from a porcine veno-arterial extracorporeal membrane oxygenation (ECMO) model [n = 9; Sus scrofa domesticus; ES breed (Schweizer Edelschwein)] with eight experimental conditions; Euvolemia [a volume state where ECMO flow produced normal mixed venous saturation (SVO2) without vascular collapse]; three levels of increasing norepinephrine infusion (Vasoconstriction 1-3); status after stopping norepinephrine (Post Vasoconstriction); and three steps of volume expansion (10 mL/kg crystalloid bolus) (Volume Expansion 1-3). In each condition, Pmsa and a "reduced-pump-speed-Pmsa" (Pmsared) were calculated from baseline and briefly reduced pump speeds, respectively. We calculated agreement for absolute values (per condition) and changes (between consecutive conditions) of Pmsa and Pmsared, against MSFP at zero ECMO flow. Euvolemia venous return driving pressure was 5.1 ± 2.0 mmHg. Bland-Altman analysis for Pmsa vs. MSFP (all conditions; 72 data pairs) showed bias (confidence interval) 0.5 (0.1-0.9) mmHg; limits of agreement (LoA) -2.7 to 3.8 mmHg. Bias for ΔPmsa vs. ΔMSFP (63 data pairs): 0.2 (-0.2 to 0.6) mmHg, LoA -3.2 to 3.6 mmHg. Bias for Pmsared vs. MSFP (72 data pairs): 0.0 (-0.3 to -0.3) mmHg; LoA -2.3 to 2.4 mmHg. Bias for ΔPmsared vs. ΔMSFP (63 data pairs) was 0.2 (-0.1 to 0.4) mmHg; LoA -1.8 to 2.1 mmHg. In conclusion, during veno-arterial ECMO, under clinically relevant levels of vasoconstriction and volume expansion, Pmsa accurately estimated absolute and changing values of MSFP, with low between-method precision. The within-method precision of Pmsa was excellent, with a least significant change of 0.15 mmHg.NEW & NOTEWORTHY This is the first study ever to validate the mean systemic pressure analog (Pmsa) against the reference mean systemic filling pressure (MSFP) determined at full arterio-venous pressure equilibrium. Using a porcine ECMO model with clinically relevant levels of vasoconstriction and volume expansion, we showed that Pmsa accurately estimated absolute and changing values of MSFP, with a poor between-method precision. The within-method precision of Pmsa was excellent.

Clinical validation of a computerized algorithm to determine mean systemic filling pressure.

Mean systemic filling pressure (Pms) is a promising parameter in determining intravascular fluid status. Pms derived from venous return curves during inspiratory holds with incremental airway pressures (Pms-Insp) estimates Pms reliably but is labor-intensive. A computerized algorithm to calculate Pms (Pmsa) at the bedside has been proposed. In previous studies Pmsa and Pms-Insp correlated well but with considerable bias. This observational study was performed to validate Pmsa with Pms-Insp in cardiac surgery patients. Cardiac output, right atrial pressure and mean arterial pressure were prospectively recorded to calculate Pmsa using a bedside monitor. Pms-Insp was calculated offline after performing inspiratory holds. Intraclass-correlation coefficient (ICC) and assessment of agreement were used to compare Pmsa with Pms-Insp. Bias, coefficient of variance (COV), precision and limits of agreement (LOA) were calculated. Proportional bias was assessed with linear regression. A high degree of inter-method reliability was found between Pmsa and Pms-Insp (ICC 0.89; 95%CI 0.72-0.96, p = 0.01) in 18 patients. Pmsa and Pms-Insp differed not significantly (11.9 mmHg, IQR 9.8-13.4 vs. 12.7 mmHg, IQR 10.5-14.4, p = 0.38). Bias was -0.502 ± 1.90 mmHg (p = 0.277). COV was 4% with LOA -4.22 - 3.22 mmHg without proportional bias. Conversion coefficient Pmsa âž” Pms-Insp was 0.94. This assessment of agreement demonstrates that the measures Pms-Insp and the computerized Pmsa-algorithm are interchangeable (bias -0.502 ± 1.90 mmHg with conversion coefficient 0.94). The choice of Pmsa is straightforward, it is non-interventional and available continuously at the bedside in contrast to Pms-Insp which is interventional and calculated off-line. Further studies should be performed to determine the place of Pmsa in the circulatory management of critically ill patients. ( www.clinicaltrials.gov ; TRN NCT04202432, release date 16-12-2019; retrospectively registered).Clinical Trial Registration www.ClinicalTrials.gov , TRN: NCT04202432, initial release date 16-12-2019 (retrospectively registered).

Mean systemic filling pressure indicates fluid responsiveness and anaesthesia-induced unstressed blood volume.

PURPOSE: The mean systemic filling pressure (Pms) plays a central role for our understanding of the circulation. In a retrospective analysis of a clinical trial, we studied whether Pms indicates fluid responsiveness and whether Pms can indicate an anaesthesia-induced increase of the unstressed blood volume, which is the volume that does not increase the transmural pressure. METHODS: An analogue to P ms based on cardiac output, the mean arterial pressure and the central venous pressure, abbreviated to P msa , were calculated in 86 patients before induction of general anaesthesia and before 3 successive bolus infusions of 3 mL kg -1 of colloid fluid. An increase in stroke volume of ≥ 10% from a bolus infusion indicated fluid responsiveness. Receiver operator characteristic (ROC) curves were used to find the optimal cut-off for P msa to indicate fluid responsiveness. Changes in blood volume were estimated from anthropometric data and the haemodilution. RESULTS: Pmsa was lower in fluid responders than in non-responders before induction (13.2 ± 2.2 vs. 14.7 ± 2.7 mmHg; mean ± SD, P < 0.01) and after induction of general anaesthesia (11.4 ± 2.1 vs. 12.8 ± 2.1 mmHg; P < 0.006). ROC curves showed that 14 mmHg before anaesthesia and 12 mmHg after anaesthesia induction served as optimal cut-offs for P msa to indicate fluid responsiveness. A linear correlation between P msa and blood volume changes suggested that the anaesthesia increased the unstressed blood volume by 1.2 L. CONCLUSIONS: P msa was lower in fluid responders than in non-responders. General anaesthesia increased the need for blood volume by 1.2 L.

Do alterations in pulmonary vascular tone result in changes in central blood volumes? An experimental study.

BACKGROUND: The effects of selective pulmonary vascular tone alterations on cardiac preload have not been previously examined. Therefore, we evaluated whether changing pulmonary vascular tone either by hypoxia or the inhalation of aerosolized prostacyclin (PGI2) altered intrathoracic or pulmonary blood volume (ITBV, PBV, respectively), both as surrogate for left ventricular preload. Additionally, the mean systemic filling pressure analogue (Pmsa) and pressure for venous return (Pvr) were calculated as surrogate of right ventricular preload. METHODS: In a randomized controlled animal study in 6 spontaneously breathing dogs, pulmonary vascular tone was increased by controlled moderate hypoxia (FiO2 about 0.10) and decreased by aerosolized PGI2. Also, inhalation of PGI2 was instituted to induce pulmonary vasodilation during normoxia and hypoxia. PBV, ITBV and circulating blood volume (Vdcirc) were measured using transpulmonary thermo-dye dilution. Pmsa and Pvr were calculated post hoc. Either the Wilcoxon-signed rank test or Friedman ANOVA test was performed. RESULTS: During hypoxia, mean pulmonary artery pressure (PAP) increased from median [IQR] 12 [8-15] to 19 [17-25] mmHg (p < 0.05). ITBV, PBV and their ratio with Vdcirc remained unaltered, which was also true for Pmsa, Pvr and cardiac output. PGI2 co-inhalation during hypoxia normalized mean PAP to 13 (12-16) mmHg (p < 0.05), but left cardiac preload surrogates unaltered. PGI2 inhalation during normoxia further decreased mean PAP to 10 (9-13) mmHg (p < 0.05) without changing any of the other investigated hemodynamic variables. CONCLUSIONS: In spontaneously breathing dogs, changes in pulmonary vascular tone altered PAP but had no effect on cardiac output, central blood volumes or their relation to circulating blood volume, nor on Pmsa and Pvr. These observations suggest that cardiac preload is preserved despite substantial alterations in right ventricular afterload.

Perioperative Hemodynamic Monitoring: An Overview of Current Methods.

Perioperative hemodynamic monitoring is an essential part of anesthetic care. In this review, we aim to give an overview of methods currently used in the clinical routine and experimental methods under development. The technical aspects of the mentioned methods are discussed briefly. This review includes methods to monitor blood pressures, for example, arterial pressure, mean systemic filling pressure and central venous pressure, and volumes, for example, global end-diastolic volume (GEDV) and extravascular lung water. In addition, monitoring blood flow (cardiac output) and fluid responsiveness (preload) will be discussed.

The inspiration hold maneuver is a reliable method to assess mean systemic filling pressure but its clinical value remains unclear.

BACKGROUND: The upstream pressure for venous return (VR) is considered to be a combined conceptual blood pressure of the systemic vessels: the mean systemic filling pressure (MSFP). The relevance of estimating the MSFP during dynamic changes of the circulation at the bedside is controversial. Herein, we studied the effect of high ventilatory pressures on the relationship between VR and central venous pressure (CVP). METHODS: In 9 healthy pigs under anaesthesia and mechanically ventilated, MSFP was estimated from extrapolated VR versus CVP relationships during inspiratory hold maneuvers (IHMs) with different levels of ventilatory pressure (Pvent). MSFP was measure 3 times per animal during euvolemia and hypovolemia. Hypovolemia was induced by bleeding with 10 mL/kg. The estimated MSFP values were compared to the blood pressure recording after induced ventricle fibrillation (i.e., mean circulatory filling pressure). RESULTS: Our results revealed a strong linear correlation between VR and CVP [R2 of 0.92 (range, 0.67-0.99)], during IHMs with different levels of Pvent. Volume status significantly alters the resulting MSFP, 20±1 and 16±2 mmHg for euvolemia and hypovolemia respectively. This estimation of the MSFP was strongly correlated-but not interchangeable-to the blood pressure recording after induced ventricle fibrillation (R2=0.8 and P=0.045). CONCLUSIONS: In conclusion, we showed a strong linear correlation between VR and CVP-when applying IHMs with high levels of Pvent-however the clinical applicability of this method to guide volume therapy in its current form is improbable.

Measurement of mean systemic filling pressure after severe hemorrhagic shock in swine anesthetized with propofol-based total intravenous anesthesia: implications for vasopressor-free resuscitation.

BACKGROUND: Mean systemic filling pressure (Pmsf) is a quantitative measurement of a patient's volume status and represents the tone of the venous reservoir. The aim of this study was to estimate Pmsf after severe hemorrhagic shock and cardiac arrest in swine anesthetized with propofol-based total intravenous anesthesia, as well as to evaluate Pmsf's association with vasopressor-free resuscitation. METHODS: Ten healthy Landrace/Large-White piglets aged 10-12 weeks with average weight 20±1 kg were used in this study. The protocol was divided into four distinct phases: stabilization, hemorrhagic, cardiac arrest, and resuscitation phases. We measured Pmsf at 5-7.5 seconds after the onset of cardiac arrest and then every 10 seconds until 1 minute postcardiac arrest. During resuscitation, lactated Ringers was infused at a rate that aimed for a mean right atrial pressure of ≤4 mm Hg. No vasopressors were used. RESULTS: The mean volume of blood removed was 860±20 ml (blood loss, ~61%) and the bleeding time was 43.2±2 minutes while all animals developed pulseless electrical activity. Mean Pmsf was 4.09±1.22 mm Hg, and no significant differences in Pmsf were found until 1 minute postcardiac arrest (4.20±0.22 mm Hg at 5-7.5 seconds and 3.72±0.23 mm Hg at 55- 57.5 seconds; P=0.102). All animals achieved return of spontaneous circulation (ROSC), with mean time to ROSC being 6.1±1.7 minutes and mean administered volume being 394±20 ml. CONCLUSIONS: For the first time, Pmsf was estimated after severe hemorrhagic shock. In this study, Pmsf remained stable during the first minute post-arrest. All animals achieved ROSC with goal-directed fluid resuscitation and no vasopressors.

Effect of volume status on the estimation of mean systemic filling pressure.

Various methods for indirect assessment of mean systemic filling pressure (MSFP) produce controversial results compared with MSFP at zero blood flow. We recently reported that the difference between MSFP at zero flow measured by right atrial balloon occlusion (MSFPRAO) and MSFP estimated using inspiratory holds depends on the volume status. We now compare three indirect estimates of MSFP with MSFPRAO in euvolemia, bleeding, and hypervolemia in a model of anesthetized pigs (n = 9) with intact circulation. MSFP was estimated using instantaneous beat-to-beat venous return during tidal ventilation (MSFPinst_VR), right atrial pressure-flow data pairs at flow nadir during inspiratory holds (MSFPnadir_hold), and a dynamic model analog adapted to pigs (MSFPa). MSFPRAO was underestimated by MSFPnadir_hold and MSFPa in all volume states. Volume status modified the difference between MSFPRAO and all indirect methods (method × volume state interaction, P ≤ 0.020). All methods tracked changes in MSFPRAO concordantly, with the lowest bias seen for MSFPa [bias (confidence interval): -0.4 (-0.7 to -0.0) mmHg]. We conclude that indirect estimates of MSFP are unreliable in this experimental setup. NEW & NOTEWORTHY For indirect estimations of MSFP using inspiratory hold maneuvers, instantaneous beat-to-beat venous return, or a dynamic model analog, the accuracy was affected by the underlying volume state. All methods investigated tracked changes in MSFPRAO concordantly.

The stop-flow arm equilibrium pressure in preoperative patients: Stressed volume and correlations with echocardiography.

BACKGROUND: The distending intravascular pressure at no flow conditions reflects the stressed volume. While this haemodynamic variable is recognised as clinically important, there is a paucity of reports of its range and responsiveness to volume expansion in patients without cardiovascular disease and no reports of correlations to echocardiographic assessments of left ventricular filling. METHODS: Twenty-seven awake (13 male), spontaneously breathing patients without any history of cardiopulmonary, vascular or renal disease were studied prior to induction of anaesthesia. The no-flow equilibrium pressure in the arm following rapid circulatory occlusion (Parm ) was measured via a radial arterial catheter. Transthoracic echocardiography was used to measure left ventricular end diastolic area and volume as well as the diameter of the inferior vena cava. The Parm and echocardiographic variables were measured before and after administration of 500 mL 0.9% NaCl over 10 minutes. Changes were analysed by paired t test, Pearson's correlation and multiple linear regression. RESULTS: Parm increased overall from 22 ± 5 mm Hg to 25 ± 6 mm Hg (mean difference 3.0 ± 4.5 mm Hg, P = 0.002) following the fluid bolus with corresponding increases in arterial pressure and echocardiographic variables. Variability in the direction of the Parm response reflected concomitant changes in vascular compliance. Only weak correlations were observed between changes in Parm and inferior vena cava diameter indexed to body surface area (R2  = 0.29, P = 0.01). CONCLUSION: Preoperative measurements of Parm increased following acute expansion of the intravascular volume. Echocardiography demonstrated poor correlation with Parm .

Application of venous return curve in hemodynamic intervention of shock patients / 中华危重病急救医学

In the cardiac output (CO) and venous return (VR) balance theory proposed by Guyton in the 1950s, the right atrial pressure (Pra) was used as the dependent variable, and the VR and right cardiac function curves were recorded simultaneously. The intersection of the two curves is the current circulating blood flow under the Pra at this moment. In patients with hemodynamically unstable shock, the primary treatment goal is to restore circulating blood volume and tissue perfusion with primary methods including fluid resuscitation and the use of vasoactive drugs. This review described the dynamic evolution of VR curve in hemodynamic intervention of shock patients and the changes in physiological indicators such as mean systemic filling pressure (Pmsf), venous resistance (Rv), and stressed volume (Vs), in order to more accurately interpret changes in hemodynamic parameters and guide the clinical treatment of shock from a goal-oriented perspective.

Determinants of systemic venous return and the impact of positive pressure ventilation.

Venous return, i.e., the blood flowing back to the heart, is driven by the pressure difference between mean systemic filling pressure and right atrial pressure (RAP). Besides cardiac function, it is the major determinant of cardiac output. Mean systemic filling pressure is a function of the vascular volume. The concept of venous return has a central role for heart lung interactions and the explanation of shock states. Mechanical ventilation during anaesthesia and critical illness may severely affect venous return by different mechanisms. In the first part of the following article, we will discuss the development of the concept of venous return, its specific components mean systemic and mean circulatory filling pressure (MCFP), RAP and resistance to venous return (RVR). We show how these pressures relate to the volume state of the circulation. Various interpretations and critiques are elucidated. In the second part, we focus on the impact of positive pressure ventilation on venous return and its components, including latest results from latest research.